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Abstract
The plant pathogen Ustilago maydis, of the Basidiomycota is responsible for corn smut disease and an important model organism for this fungal phylum. One of the main aims in our laboratory is to investigate the genetic determinants involved in the processes associated with U. maydis morphogenesis and pathogenic development. In the work reported here, I was particularly interested in addressing the roles of autophagy and the regulation of cell wall degrading enzymes (CWDE) as key controlling factors of U. maydis development and virulence. Using a reverse genetic approach and a combination of other techniques, we firstly showed here that the U. maydis autophagy related genes atg1 and atg8, are associated with autophagy dependent processes. Deletion of atg8 resulted in a lower survival capacity during carbon starvation conditions, abnormal morphogenesis, and most importantly severe reduction of virulence. Interestingly, atg1 strains yielded phenotypes similar to the atg8 strains but of lower magnitude. Surprisingly, atg1 deletion in the atg8 background generated an additive phenotype.We then focused on the study of U. maydis CWDE genes as potential virulence factors regulated by carbon source availability. Little is known about the mode that U. maydis employsto penetrate and spread in the corn plant and CWDE involvement in these processes has been hypothesized but never thoroughly tested. CWDE genes in fungi are often subject to transcriptional glucose repression. In yeast, one of the main players controlling this process is SNF1, which encodes a protein kinase. SNF1 homologue disruption in the phytopathogenic fungi Fusarium oxysporum and Cochliobolus carbonum led to a reduction in the expression of several CWDE genes accompanied by a decrease in virulence. In this work we showed that in U. maydis Snf1 acts as either a negative or positive regulator of particular CWDE genes and is not required for metabolism of alternative carbon sources. Unlike in Ascomycete plant pathogens, deletion of snf1 did not profoundly affect virulence in U. maydis.